Insulin shifts the steady state subcellular distribution of IGF-II receptors from a large intracellular pool to the plasma membrane in the rat adipose cell. In the present study, the counterregulatory effects of adrenergic stimulation, adenosine deaminase (ADA), and cAMP on this process have been studied. The results suggest that beta-adrenergic stimulation, through a cAMP-dependent mechanism, markedly alters the insulin-stimulated redistribution of IGF-II receptors. This effect is additional to the potent antagonistic action of cAMP on insulin's signaling mechanism. We have also examined the modulation of protein kinase C-mediated stimulation of glucose transport activity in the rat adipose cell by 1) ligands for receptors that mediate stimulation (R(s); lipolytic) or inhibition (R(i); antilipolytic) of adenylate cyclase and 2) pertussis and cholera toxins which regulate the inhibitory (G(i)) and stimulatory (G(i)) and stimulatory (G(s),) guanyl nucleotide-binding proteins of adenylate cyclase, respectively. The results suggest that 1) C-proteins modulate protein kinase C-mediated stimulation of glucose transport activity by altering the intrinsic activity of glucose transporters residing in the plasma membrane and 2) a functional G(i) protein is required for stimulation of glucose transport activity by phorbol esters and vasopressin.